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Pituitary gland – Pituitary fossa • Mass: 5 gms • DIMENSIONS – 7mm (Ht) – 9mm (AP) – 11m(transverse) originates from Rathke’s pouch and infundibulum Cell type hormone Clinical syndrome Tumor type Somatotroph Growth Hormone Acromeg/gigan Sparsely granulated GH cell Densely granulated GH cell Lactotroph Prolactin Amen/galactor Sparsely granulated prl Densely granulated prl Somato/Lact Corticotroph Gh+prl Acth/Pomc /B-lph/Msh Acro+hyperprl Mixed GH-prl Acro+hyperprl Mammo+somato Amen/Gal/Acro Acido+stem cell Cushings, nelson Densely granulated acth Sparsely granulated acth Gonadotroph FSH,LH,ASub Unit Hypopituitarism Gonadotroph Thyrotroph TSH, A-sub Unit Hyperthyroid/ Hypopituitarism Thyrotroph NULL Cell None Hypopituitarism Null cell oncocytoma 15% of intracranial tumors Present as incidental finding in 5-20% Broadly divided (a) functional (b) non functional History and physical examination Neuro- ophthalmology: Acuity, field, fundus and movements Hormone levels Basal hormone and dynamic testing Aim- hypersecretory state or insufficiency Radiology (a) X-Rays (b) MRI (c) NCCT/CECT Routine blood investigation Mass effect Hyper secretion/ hypo secretion Incidental finding Apoplexy Complete history and physical examination Eyes – visual acuity, visual field, fundoscopy Neck- thyroid ,carotid bruit Chest-gynaecomastia, galactorrhea Abdomen-striae, obesity Extremities-edema, enlargement Skin-pigment, hair, bruises Visual disturbances – Visual field defect usually very insidious and slowly progressive – Diplopia – Visual acuity Hydrocephalus Headache Cranial nerve palsies Raised intracranial pressure Apoplexy – – – – – Acute presentation secondary to tumour haemorrhagic necrosis Headache Vomiting Blindness Ocular paresis Altered level of consciousness Prolactin Galactorrhoea , amennorrhoea, osteoporosis G.H Acromegaly, organomegaly, D.M, ACTH Cushing’s disease, Diabetes mellitus, osteoporosis, obesity, hypertension TSH Hyperthyroidism, cardiac dysrhythmia, heat intolerance X- Rays: Widening of sella Destruction of sellar floor Relation of median sphenoidal septum Aeration of sphenoid sinus- conchal sclerotic mixed NCCT+ CECT head/ sella with thin coronal cuts: findings as seen in X-Rays iso dense to adjacent brain parenchyma intense contrast enhancement calcifications uncommon (< 5%) apoplexy- hyper density MRI brain: Sagittal T!WI and coronal T1WI sellar and parasellar region with/without contrast 2.5mm thin contiguous slices and 5mm slices axial T2WI of whole brain. Normal pituitary is iso intense to gray matter on T1WI with contrast enhancing Pituitary adenoma classified based on size: microadenoma <10mm macroadenoma >10mm giant pit adenoma >40mm Macro adenoma – Micro adenomas- they are hypo to isointense to gray matter on T1WI, contrast enhancing Dynamic contrast study done by 5 T1WI turbo spin 3mm thin slices repetitively at 20,40,60,80,100 sec after 10ml contrast injection at 2ml/sec. Micro adenoma enhance and wash out quickly as compared to normal gland post contrast and hence appear hypointense deviation of stalk bulging of inferior and superior margin Signal Intensity Normal Gland Adenoma t0 Time tx Pituitary adenoma: Grade Grade Grade Grade Grade Grade 012345- size < 10 mm, sella normal size < 10 mm, sella expanded size > 10 mm , sella expanded size > 10 mm, focal Destruction size > 10 mm, diffuse destruction distant spread Suprasellar 0- none A- supra sellar cistern B- ant recess of third ventricle obliterated C- floor of third ventricle grossly displaced Parasellar D- intracranial (intradural) E- into or beneath the cavernous sinus Hormone excess serum prolactin serum IGF-1 serum LH, FSH serum A sub unit serum TSH urinary24 hr cortisol Hormone deficiency serum cortisol serum T4, free T3 serum testosterone (men) serum estradiol (women) Dynamic stimulation/suppression testing may be useful in select cases to further evaluate pituitary reserve and/or for pituitary hyperfunction Acromegaly Oral glucose test- Cushings syndrome/disease- (a)low dose dexamethasone (b)low dose dexamethasone +CRH (c)high dose dexamethasone (d)Inferior petrous sampling + CRH ACTH – low dose ACTH by giving 1 mcg iv and S. cortisol after 30 min less than 18 mcg/dl identifies central adrenal deficiency 30 to 50% of endocrine active tumors Clinical features: Amennorhoea infertility, loss of libido, oligospermia Galactorrhoea in 80% females and 30% men Majority are microadenomas 30% of them in women are self limiting Prolactin < 25 ng/ ml normal 25- 150ng/ml prolactinoma, stalk effect, drugs , Hypothyroid > 150ng/ml- prolactinoma Hook effect- even large elevations will show normal PRL levels on testing due to large size of molecules. Do serial dilutions Not all hyperprolactinemia is due to a prolactinoma Causes of Hyperprolactinemia Medications Psychotropic (e.g.. haloperidol. resperidol) Antidepressants (e.g.. amoxapin) Estrogen Opiates Calcium channel blocker (veraparnil) Antihypertensives (a methyldopa. reserpine) Dopamine antagonists (domperidome. metoclopramide) Pituitary Pituitary adenoma Prolactin-secreting adenoma GH-secreting adenoma Secondary hyperprolactinemia. usually a macroadenoma Other pituitary lesion. e.g.. inetastatic. sarcoid. aneurysm Hypothalamic lesion Head trauma Pregnancy Spinal cord lesions Chest wall trauma Nipple stimulation 15% of all pituitary adenomas in adults 90% microadenomas Common in women 55 % pit adenoma in children Clinical features: Central obesity, purple striae, hypertension, diabetes, ecchymosis, poor wound healing, lipid abnormalities, neuropsyhiatric problems Best screening test- 24 hr UFC level 95-100% sensitivity, 400 mcg/day of UFC is diagnostic. midnight plasma cortisol of 5.2mcg/dl is diagnostic of cushings Low dose dexamethasone test- 1 mg of dexa at 11.00 am and measurement of s. cortisol at 8.00 am <5 mcg/dl- normal 5-10 mcg/dl equivocal >10mcg diagnostic Plasma corticotropin level- >20pg/ml diagnostic >10 pg/ml suggestive <5pg/ml corticotroph independent High dose dexa suppression 8 mg dexamethasone test -8 mg dexamethasone is test- if corticotrops >10 pg/ml . 2mg of dexa given every 6hrly for 2 days, if > 69% fall in 24 hr UFC (pre and post dexa ) is 100% specific for CD given at 11.00 pm and drop in >50% s. cortisol indicates CD Corticotropin releasing hormone stimulation test- I mcg/kg CRH iv in morning, if increases >35% corticotropin level at 15, 30 min above baseline yields 100% specificity and 93% sensitivity for CD Inferior petrosal sinus sampling classical clinical and biochemical CD features with MRI negative patient equivocal suppression and stimulation test Diagnostic accuracy is 80-100% , blood samples are obtained at basal and 3,5,10 min after CRH administration and ips/ps ratio calculated ips/ps >3 CD ips/ps <2 ectopic rarely 2-3 ectopic IPS gradient helps in lateralization of adenoma 4th decade of life 10.7 years Constitute 20% of all pituitary tumors Preop duration 10 years to diagnosis in adults and 3.1 years in children Pleuri hormonal Prepuberty-gigantism & precocious puberty Pubescent-amenorrhea, hypogonadism Adults-skeletal and soft tissue overgrowth and deformities, cardiac ,neuromuscular, respiratory, endocrine, metabolic complications and neoplastic transformation Random GH – negative results not useful gives false positive and false Insulin like growth factor 1 (IGF-1) – best for screening represents average daily GH secretion Oral glucose GH suppression testing – GHRH stimulation test gold standard to confirm diagnosis :75 mg of glucose load normally suppresses GH > 2ng/ml RIA. GH nadir >2ng/ml RIA with adenoma confirms it Chest and abdomen imaging for ectopic GHRH secreting tumors Empty sella shows pituitary infarction Scintigraphy Ancillary tests Blood glucose, urine, cardiac and respiratory Screening for colorectal neoplasia Clinically Acromegaly, MRI pit adenoma, GH>5ng/ml If GH<5ng/ml IGF-1, elevated If no Oral glucose suppression test confirms it rarely MRI negative , measure GHRH levels, CECT abd /chest TSH secreting tumors 1-2% of pit adenomas Mixed hormonal secretion- 30% GH, PRL, Gonadotropins 90% macroadenomas Mean duration pt 9 yrs Clinical features of goitre, warm skin, heat intolerance, cardiac arrhythmias and other hyperthyroid features, Lab investigations TSH, Free t4,t3by direct method a-subunit, PRL, GH, SHB Iodine scan/USG of thyroid Dynamic testing with TRH Clinical suspicion, MRI –pit adenoma, baseline TSH, free T4/T3,a-sub unit,PRL,GH TSH normal, a-sub unit/TSH ratio <5.7 in normogonads,<29.1 in hypergonad, TSH elevated<0.7 in normogonads, <1.0 in hypergonads MRI equivocal, TRH stimulation test 7-15% of pit adenomas 40-50 % macroadenomas secrete gonadotropins Clinical features of mass effect: visual symptoms, hypogonadism, amennorrhea, hypothyroid, hypocortisolism Lab investigations basal hormonal levels TRH stimulated gonadotropins, and sub units normally causes absent FSH response and no more than 33% increase in LH and b- LH primary hypogonadism LH,FSH elevated and don’t respond to TRH gonadotropinomas have greater than 60% increase in b-LH levels Hormonal status-endocrinologist Visual field –orthoptist Monitor tumor recurrence –radiologist Clinical observation-neurosurgeon Blood test-biochemist THANK YOU